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Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
Published on: January 26, 2018
Keep calm and carry H3K27me1 off.
Rafael Alcalá-Vida1, Angel Barco1
1Instituto de Neurociencias, Universidad Miguel Hernández - Consejo Superior de Investigaciones Científicas, Av. Santiago Ramón y Cajal s/n. Sant Joan d'Alacant, 03550 Alicante, Spain.
Stress-susceptible mice show increased H3K27me1 epigenetic marks in the nucleus accumbens. This finding links specific epigenetic changes to lasting social, emotional, and cognitive alterations caused by stress.
Area of Science:
- Neuroscience
- Epigenetics
- Behavioral Science
Background:
- Stress-induced alterations in social, emotional, and cognitive functions are significant.
- Epigenetic modifications are increasingly recognized as mediators of long-term behavioral changes.
Purpose of the Study:
- To investigate the specific epigenetic changes in the nucleus accumbens of stress-susceptible mice.
- To elucidate the role of the SUZ12 VEFS domain in stress-induced epigenetic alterations.
Main Methods:
- Analysis of histone modifications, specifically H3K27me1 levels.
- Focus on neurons within the nucleus accumbens.
- Utilizing a mouse model of stress susceptibility.
Main Results:
- Stress-susceptible mice displayed elevated levels of H3K27me1 in nucleus accumbens neurons.
- The SUZ12 VEFS domain was implicated in mediating these observed epigenetic changes.
Conclusions:
- Specific epigenetic changes, such as elevated H3K27me1, are associated with stress susceptibility.
- These epigenetic alterations contribute to long-lasting social, emotional, and cognitive deficits following stress exposure.
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